Respiratory burst of turbot (Scophthalmus maximus) macrophages in response to experimental infection with viral haemorrhagic septicaemia virus (VHSV)

Viral haemorrhagic septicaemia is a severe fish disease caused by a rhabdovirus, viral haemorrhagic septicaemia virus (VHSV). Although it usually affects salmonids, some marine species like turbot (Scophthalmus maximus) are also susceptible to the disease (Schlotfeldt et al., 1991; Ross et al., 1994). Only a few studies have focused on the pathogenesis and defence mechanisms implicated in this disease. It is already known that VHSV replicates in turbot kidney macrophages (Tafalla et al., 1998) as it does in kidney macrophages from other species (Estepa et al., 1992). As macrophages are one of the principal defence elements against viral infection (Gendelman & Morahan, 1992), it is important to determine which immune mechanisms are triggered by macrophages in viral infections. Moreover, it is also important to determine which macrophage functions are suppressed because of infection. Macrophages play an important role in non-specific resistance to different infections, acting directly against the pathogen by releasing reactive oxygen and nitrogen intermediates, phagocytosing foreign particles, or producing cytokines that affect the response of other cells in the immune system. Previous studies in mammals have revealed that viral infections may trigger the macrophage production of reactive oxygen intermediates, as well as nitric oxide (NO) (Akaike et al., 1998). Concerning VHSV, in vitro experiments have shown that the virus does not significantly affect the respiratory burst activity of turbot macrophages (Tafalla et al., 1998). Exogenous NO, however, is known to suppress VHSV replication significantly in turbot head-kidney macrophages (Tafalla et al., 1999). However, in order to understand the pathogenesis and prevent or treat the infections, it is important to determine the effects of fish pathogens in vivo, because within the host many factors and cell types may be implicated. In this work, the release of oxygen intermediates (respiratory burst activity) by turbot macrophages after in vivo infection with VHSV has been determined, as well as the NO concentration in plasma. The effect of serum derived from VHSV-infected turbot on both macrophages respiratory burst and NO production was also studied.